Pathophysiology of coronary artery disease

Atherogenic risk factors provoke chronic injury to the endothelium in certain parts of the arterial tree leading to dysfunctional endothelium. Lipid accumulation, macrophage formation, and smooth muscle cell proliferation are key events in the initial slow progression of atherosclerotic lesions (phase 1). If extracellular lipid accumulation predominates, atherosclerotic process progresses into a more clinically relevant, advance lipid-rich lesion (phase 2)-the pathogenic basis for plaque rupture and thrombus formation. Small plaque fissures and mural thrombus formation may be responsible for the rapid, clinically silent progression of lesions (phase 3). Plaque rupture with large thrombus formation may be responsible for acute coronary syndromes (phase 4). Alternatively, if smooth muscle cell proliferation and collagen matrix synthesis predominate, atherosclerotic lesions may progress into advanced, stable sclerotic lesions (phase 5).